Classification of chronic hepatitis: Diagnosis, grading and staging

Desmet, V J

doi:10.1016/0270-9139(94)90250-x

Cited by 747 publications

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“…CT/MRI was also performed when there was an abnormal elevation in an HCC-specific tumor marker while ultrasound findings were negative. In most patients, ultrasound-guided liver biopsy was also performed and histology was evaluated according to the classification of Desmet et al [19].…”

Section: Diagnosis Of Hccmentioning

confidence: 99%

Ultrasound surveillance for early detection of hepatocellular carcinoma among patients with chronic hepatitis C

et al. 2009

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Background and aims Ultrasonography is the most frequently used modality in surveillance for HCC among patients with chronic hepatitis C. However, the optimal surveillance interval is still controversial and the usefulness of supplementary tumor marker determination has not been confirmed. Methods A total of 243 cases of naive HCC were detected among 1,431 patients with chronic hepatitis C under outpatient-based surveillance. The mode of HCC detection, including ultrasound surveillance interval, was retrospectively examined and the relation between the interval and detected tumor size was analyzed. Tumor volume doubling time was estimated from exponential increase in serum tumor marker levels when applicable. Results HCC was first detected by ultrasonography in 221 patients. Ultrasound surveillance interval, ranging between 2 and 8 months, was not correlated with the size of tumor at detection. Patients with cirrhosis were likely to be surveyed at shorter intervals. The size of tumor exceeded 30 mm only in three (1.4%) cases. They were all positive for a biomarker and the estimated tumor doubling time was short. In 14 cases, HCC was first detected by CT indicated by abnormal rise in tumor marker levels despite negative ultrasound findings. In the remaining eight cases, ultrasonography had been replaced by CT as surveillance modality because of excessive obesity or coarseness of liver parenchyma.Conclusions Ultrasound surveillance at 6-month intervals was appropriate in general for the detection of HCC at a size smaller than 30 mm. However, in patient with established cirrhosis, more frequent screening would be needed to detect tumors of the same size.

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Section: Diagnosis Of Hccmentioning

confidence: 99%

Ultrasound surveillance for early detection of hepatocellular carcinoma among patients with chronic hepatitis C

et al. 2009

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“…who was unaware of the patients' clinical condition. The degree of fibrosis and the intensity of inflammatory activity were graded according to the scoring system described by Desmet et al 8 with slight modification: F0, F1, F2, F3, and F4 were defined as none or minimal fibrosis, fibrous portal expansion, bridging fibrosis (portal-portal or portal-central linkage), bridging fibrosis with lobular distortion, and cirrhosis, respectively. F0, F1, and F2 were defined as "mild fibrosis" and F3 and F4 were termed "severe fibrosis" in the current report.…”

Section: Histologic Examinationmentioning

confidence: 99%

Impact of aging on the development of hepatocellular carcinoma in patients with posttransfusion chronic hepatitis C

Hamada

Yatsuhashi

Yano

et al. 2002

Cancer

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BACKGROUNDHepatitis C virus (HCV) infection is a heterogeneous disease, the natural history of which remains controversial. There is solid evidence that chronic HCV infection is responsible for the occurrence of hepatocellular carcinoma (HCC). The aim of the current cohort study was to determine the rate of the development of HCC from the time of primary HCV infection and to assess the risk factors for the development of HCC in chronic posttransfusion hepatitis C patients.METHODSFour hundred sixty‐nine patients with clinically compensated HCV, who had undergone a single blood transfusion comprised the current study cohort. Patients with other risk factors for chronic liver disease were excluded. All patients were referred to the liver center at the National Nagasaki Medical Center between December 1980 and December 1998 and were followed prospectively until the end of the analysis (June 2000).RESULTSFollow‐up data were obtained for 445 patients. The mean duration from HCV infection to the end of the observation was 28 years. Fifty‐two patients (11.1%) progressed to HCC. The mean duration from the time of blood transfusion to the diagnosis of HCC was 31 years. Multivariate Cox regression analyses revealed age, fibrosis, duration from HCV infection to study entry, and alcohol consumption to be the independent factors affecting the development of HCC. The risk of developing HCC in patients age ≥ 56 years was increased 7.8‐fold compared with that in patients age < 56 years. The mean age of patients at the time of HCC diagnosis was 65 years (range, 58–79 years).CONCLUSIONSAt the time of diagnosis, 92% of the 52 HCC patients were age > 60 years and 38 of the HCC patients (73%) were in their 60s. There was a significantly negative correlation between the duration from HCV infection to the development of HCC and the age of the patient at the time of infection (correlation coefficient = 0.702; P < 0.0001; Y = 61.1–0.82X), indicating that the age of patients, rather than the duration of HCV infection, is more significant for HCC development in patients with posttransfusion HCV. Moreover, these data may contribute to the design of an optimal follow‐up schedule for patients with posttransfusion HCV. Cancer 2002;95:331–9. © 2002 American Cancer Society.DOI 10.1002/cncr.10662

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“…Thin sections (approximately 4 µm) were stained with hematoxylin and eosin, with Van Gieson, with diastasePeriodic Acid-Schiff and with Prussian blue. Grading of necroinflammatory activity (0 to 18) and staging of fibrosis (0 to 4) were semiquantitatively assessed using the Knodell scoring system, as modified by Desmet et al 19 The following histological parameters were also considered: steatosis (absent ϭ 0; mild ϭ 1; marked ϭ 2), bile duct lesions (present or absent), and follicular lymphomonocytic infiltrate (present or absent). Bile duct damage was defined as vacuolated acidophilic cytoplasm with nuclear pyknosis and the presence of inflammatory cell migration into or between the epithelial cells.…”

Section: Histological Assessmentmentioning

confidence: 99%

Liver cell apoptosis in chronic hepatitis C correlates with histological but not biochemical activity or serum HCV-RNA levels

et al. 2000

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In hepatitis C virus (HCV) infection, mechanisms responsible for liver cell damage are still poorly understood and both necrosis and apoptosis may be operative. By using terminal deoxynucleotydil transferase-mediated d-UTPbiotin nick-end labeling (TUNEL) we have evaluated and quantified apoptosis in liver biopsy specimens from 61 patients with chronic hepatitis C. All patients had detectable apoptotic cells in the liver. Presence of increased apoptotic activity was confirmed in selected cases by electron microscopy and by DNA gel electrophoresis. The amount of liver cell apoptosis expressed as apoptotic index, ranged between 0.01% to 0.54% and showed a positive correlation with histological activity grading (P F .0005) and with the amount of infiltrating CD8-positive cells (P ‫؍‬ Hepatitis C virus (HCV) is a major cause of chronic liver disease, cirrhosis, and hepatocellular carcinoma 1 worldwide. The infection has a high propensity to chronicity and the majority of HCV carriers have histological evidence of liver inflammation and chronic damage, although with a very wide spectrum of severity and progression rate. 2 The mechanisms leading to liver cell injury, inflammation, and fibrosis in chronic hepatitis C, are not fully understood. Both immunemediated reactions and more direct cytopathic effects of HCV and of its proteins may be involved. Evidence has been provided that apoptosis of liver cells may play a significant role in the pathogenesis of hepatitis C. [3][4][5] Apoptosis is an active, genetically programmed phenomenon of cell death characterized by a unique sequence of events, with morphological features distinct from necrosis. 6 Three pathomorphologic features are suggestive of increased apoptosis in the liver of patients with chronic hepatitis C including (1) presence of shrinkage and fragmentation of nucleus/cytoplasm in areas of piecemeal necrosis, (2) presence of acidophilic bodies, and (3) focal cell drop out in the liver lobule. 7,8 Increased expression of Fas, one of the most important members of the tumor necrosis factor family receptors able to transduce the apoptotic signal to programmed cell death, has been described in chronic hepatitis C. Hepatic up-regulation of Fas was found to correlate with more severe inflammation 9 and with ongoing HCV infection. 10 Parallel activation of T lymphocytes expressing Fas ligand was detected in liver infiltrating mononuclear cells, allowing transduction of the apoptotic death signal to Fas-bearing hepatocytes 3 and to proinflammatory activated cells that continuously migrate from extrahepatic sites. 11 In addition, both structural and nonstructural HCV proteins have been shown to interact with apoptosis mediators and possibly modulate the active cascade of events leading to programmed cell death. The core protein has shown both proapoptotic or antiapoptotic activities, depending of the experimental conditions and type of cell used, 12-14 whereas both the NS3 15 and the NS5A 16 proteins were shown to have antiapoptotic effects. In this study we have quant...

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Classification of chronic hepatitis: Diagnosis, grading and staging

Cited by 747 publications

References 0 publications

Ultrasound surveillance for early detection of hepatocellular carcinoma among patients with chronic hepatitis C

Ultrasound surveillance for early detection of hepatocellular carcinoma among patients with chronic hepatitis C

Impact of aging on the development of hepatocellular carcinoma in patients with posttransfusion chronic hepatitis C

Liver cell apoptosis in chronic hepatitis C correlates with histological but not biochemical activity or serum HCV-RNA levels

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